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Cardiac Resuscitation Flashcards

1
Q

Cardiac anatomy

A

myocardium - cardiac muscle, made of cardiomyocytes

Pericardium - outermost layer of heart
Pericardial sac - Fluid-filled sac surrounding heart

Coronary circulation is mechanism for perfusion of the myocardium.

Endocardium - innermost layer of heart

4 heart chambers: 2 atria and 2 ventricles

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2
Q

Cardiac output

A

4-8 L/min
average adult is 5.5

Q = HR x SV

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3
Q

Heart valves

A

tricuspid (right) and mitral valves (left) allow blood into ventricles. Open and close at same time.

pulmonic (left) and aortic valves (right) allow blood out of ventricles. Semilunar valves. Open and close at same time.

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4
Q

Tricuspid valve

A

3-leaf, low-pressure valve. AV valve
Separates right atrium from right ventricle

Right atrial pressure (central venous pressure): 2-6 mmHg

Right ventricular pressure: 0-5 mmHg

80% of preload is reliant on the function of the AV node, allowing for passive flow.

Remaining 20% of preload is from atrial contraction.

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5
Q

Pulmonic valve (semilunar)

A

Maintains diastolic pressure
Separates right ventricle from pulmonary artery (only artery to carry deoxygenated blood).

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6
Q

Mitral valve (aka bicuspid)

A

bicuspid valve (2 cusps). AV Valve.
Separates left atrium from left ventricle
High pressure valve

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7
Q

Aortic valve (semilunar)

A

most important to maintain cardiac output
Separates left ventricle from aorta/body
preload dependent

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8
Q

heart pressures (L vs R)

A

left side: high pressure
right side: low pressure

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9
Q

cardiac cycle anatomy

A

SA node fires, tricuspid valve opens, passive filling of blood from right atrium into right ventricle (diastole).

AV node slows conduction long enough for preload to happen passively.

After right ventricle fills, tricuspid valve closes and first phase of preload is complete. S1 sound.

Next, blood moves out of right ventricle through pulmonic valve to pulmonary artery (to lungs for oxygenation). This squeezing of the ventricles to eject blood out of heart is called isovolumetric contraction. When semilunar valves close, S2 sound.

Blood returns to left atrium from lungs via the pulmonary veins (left atrial preload).

Blood moves to from left atrium to left ventricle (high pressure side) through mitral valve.

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10
Q

Diastole

A

heart at rest
During diastole, blood fills right atrium from inferior and superior vena cava.
Blood also fills left atrium from pulmonary veins.
Coronary arteries and heart muscle are perfused.

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11
Q

systole

A

cardiac contraction phase
no cardiac perfusion

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12
Q

SA node rate

A

Sinoatrial node - primary pacemaker
60-100 bpm

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13
Q

AV node rate

A

Atrioventricular node - secondary pacemaker

40-60 bpm

AV node delays conduction for RV filling

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14
Q

Heart tones

A

S1
Mitral and tricuspid closure (AV)
…“lub” sound

S2
Aortic and pulmonic closure (semilunar)
…“dub” sound

S3
passive LV filling, striking compliant LV
Found in athletes with high cardiac output
“Ken-TUCKy” sound

S4 - Active LV filling when atrial contraction forces blood into a noncompliant left ventricle.
…pathalogic. “Ten-nessee”

Cardiac physiology part 2

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15
Q

Cardiac Conduction

A

SA node
AV node
Bundle of His
Right bundle branch
Left bundle branch
…left posterior fascicle
…left anterior fascicle. Most common for conduction problem
Purkinje fibers: 15-40 bpm

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16
Q

cardiac cycle electrophysiology

A

P-wave: depolarization of atria in response to SA node firing (atria contracts). Bump up on EKG

PR interval: delay of AV node allowing RV to fill. Flat on EKG while electrical signal passes through AV node.

Q-wave: septal depolarization (depolarization moving through bundle branches). Short sharp bump down on EKG

R-wave: ventricular depolarization

QRS Complex: depolarization of the ventricles which triggers pumping contraction…blood leaves right ventricle into pulmonic valve OR blood leaves left ventricle into aorta to body.

ST segment - beginning of ventricle repolarization

T-wave: ventricular repolarization (re-setting of the heart so it can fire again)

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17
Q

Path of blood through heart/body

A

Deoxygenated blood enters RIGHT ATRIUM from inferior and superior vena cava

Blood flows from RIGHT ATRIUM through tricuspid valve into right ventricle

RIGHT VENTRICLE pumps deoxygenated blood through pulmonary valve into pulmonary artery and on to the lungs.

Blood is oxygenated in lungs

Oxygenated blood from lungs returns to heart through pulmonary veins into LEFT ATRIUM.

Blood flows from left atrium through mitral valve into LEFT VENTRICLE.

Left ventricle pumps oxygenated blood through aorta to rest of body.

Then deoxygenated blood returns to right atrium and process starts over.

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18
Q

Atrioventricular (AV) valves

A

Tricuspid and mitral (bicuspid).

Tricuspid separates RA and RV.

Mitral (bicuspid) separates LA and LV.

AV valves are open during diastole and closed during systole to prevent regurgitation.

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19
Q

Semilunar valves

A

Aortic and pulmonic

Aortic separates LV and aorta

Pulmonary separates RV and pulmonary artery.

Semilunar valves are open during systole and closed during diastole

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20
Q

J-point

A

start of ST segment.
Normal J-point is at isoelectric line
J-point below line = ischemia
J-point above line = pt progressing in disease process.

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21
Q

right coronary artery

A

comes off of aorta
blood flow to RCA during diastole when aortic valve is closed.
Supplies blood to right ventricle, right atrium, SA node, and AV node.
Supplies inferior wall, posterior wall.
Most of anterior heart
Occlusion causes changes such as 1st and 2nd degree AV blocks and Mobitz type 1.

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22
Q

Left coronary artery

A

Circulation during diastole.
Feeds high and low lateral wall.
Left anterior descending - anterior surface of left ventricle.
Supplies blood to left atrium and left ventricle.

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23
Q

New systolic murmur after inferior MI

A

Most recent cause - mitral regurgitation

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24
Q

Posterior wall MI

A

Depression or reciprocal changes in nV2-V4 w/associated inferior wall MI (II, III, aVF)

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25
RCA leads on EKG
II, III, aVF Inferior
26
Left main / LAD leads on EKG
V1, V2, V3, V4 Anterior
27
LCx Branch leads on EKG
I, aVL, (High lateral) V5, V6 (lower lateral)
28
Left Main insufficiency on EKG
aVR
29
inferior leads on EKG
II, III, aVF
30
Anterior leads on EKG
V1, V2, V3, V4
31
Collateral Circulation
Vessels created to provide an alternate route of circulation to distal areas of the heart. ...Usually presents as a result of aging.
32
Ramus Intermedius
20-30% of population has this branch. Lateral wall vessel
33
Evolution of Occlusion MI (hyper acute)
Early changes suggestive of OMI Tall and peaked T-waves ...T-waves should be asymmetric. ...symmetrical T waves indicate ischemia May precede clinical symptoms Only seen in Leeds looking at infarction areas Not used as a diagnostic finding.
34
Evolution of Occlusion MI (Acute)
ST segment elevation (1-2mm elevation) Implies myocardial injury occurring Elevated ST segment presumed acute rather than old. Physiologic Q wave: <0.04 sec or <1mm wide <1/3 R wave height or <2mm deep Pathologic Q wave: Pathologic = late finding and/or old injury >0.04 sec or >1mm wide >1/3 R wave height or >2mm deep All Q waves in V2-V3
35
Coronary arteries (2 main)
Right and left coronary arteries branch from aorta
36
Left coronary artery
Branches into: 1. Left anterior descending (LAD) Multiple septal branches off of LAD Septal branches perfuse intrarventricular septum Also multiple diagonal branches off of LAD Diagonal branches perfuse Anteriolateral left ventricle. 2. Left circumflex (LCX) Wraps around circumference of heart. First branch off of LCX is left atrial artery to perfuse left atrium. Next branch is obtuse (left) marginal artery 3rd branch (not everybody). Ramus perfuses anterior lateral wall.
37
Right Coronary Artery
Comes from right side of aorta Perfuses right atrium, right atrium, SA and AV nodes 1st branch: Conus artery 2nd: Sinoatrial nodal artery: perfuses SA node 3rd: right atrial branch. Perfuses right atrium 4th: Acute marginal artery. Perfuses right ventricle. wraps around to back of heart, then... Atrioventricular nodal artery: perfuses AV node RCA then bifurcates: Right posteriolateral artery (RPL): inferiolateral / posteriolateral wall Posterior Descending Artery (PDA): perfuses inferior / posterior wall - left and right ventricle. RCA on EKG: II, III, aVF (inferior leads)
38
Coronary Sinus (vein)
Drains deoxygenated blood back into right atrium
39
EKG interpretation approach
1. Look at V1 to r/in or r/out BBB 2. Look for ST elevation segments ...(1, aVL), then (II, III, aVF), then (V1 - V5) 3. Look for reciprocal changes ...aVL and III are twins, mimic each other ...When both have ST elevation it's confirmation of a high lateral wall MI
40
Bundle branch block
QRS > 120 mS or 0.12
41
Symmetrical T-waves
Indicate ischemia
42
Inferior wall MI (preload)
Preload problem Often right ventricular infarction (RVI)
43
LEOPARD (EKG)
Left ventricular hypertrophy Early depolarization Osborn waves Pericarditis Aberrant Conduction (LBBB) Raised ICP Device (Paced rhythm)
44
Left Ventricular Hypertrophy (EKG)
LVH recognition = kissing QRS ...Deep QS waves that move deep into lead below. S wave depth in V1 plus tallest R wave in V5-V6. >35mm diagnostic for LVH aVL R wave > 11mm = LVH aVF R wave > 20mm = LVH Only 1 of these indications needs to be positive to identify LVH. If positive for LVH, pt probably not a candidate for STEMI activation
45
Early (benign) repolarization (EKG)
Common in black males 20-40 yrs old Normal physiology. Tall waves
46
Osborn waves (EKG)
(osborn) J wave morphology first identified in hypothermia (<30C) Indicative of a slow deflection of uncertain origin. Also seen in hypercalcemia, secondary to hyperparathyroidism >3.4 mmol/L or >14 mg/dL
47
Pericarditis (EKG)
Pericarditis = inflammation of pericardial sac. Sharp chest pain radiates to base of neck pts unable to lay supine often recent viral illness ST elevation throughout 12-lead ekg (as opposed to specific area of heart) PR intervals are down-sloping (tell-tale sign of pericarditis)
48
Aberrant Conduction (EKG)
BBB criteria = V1 QRS > 0.12 or 120ms Negatively deflected QRS = LBBB Positively deflected QRS = RBBB Old vs new LBBB will cause ST elevation but pt may not need Cath lab
49
Raised ICP (EKG)
High sympathetic tone Increased norepinephrine leads to (deep, >10mm) inverted t-waves
50
Device (paced) (EKG)
R wave progression ...Negative R wave deflection in V1, but by V6, ...(?) Wide QRS across EKG Looks like ST elevation
51
WALDO
Wellen's syndrome aVR lead abnormalities LBBB De Winter's T wave Out of Hospital ROSC
52
Wellen's Syndrome (EKG)
...pain free ...normal to slight elevation in cardiac markers ...biphasic t waves in V2-V3 (2 angles) Deep symmetric t waves in precordial leads Severe Proximal LAD stenosis >75% pts will proceed to anterior wall MI within a few weeks. NO significant ST elevation occurs. Type 1: uploading ST. Biphasic t-wave V2-3 Type 2: negative and symmetric t-wave WALDO
53
aVR (diagnostic) (EKG)
ST elevation in aVR that's greater than ST elevation in V1, AND anterior depression, that's highly suggestive of left main insufficiency. Often progresses to significant MI if not treated. WALDO
54
LBBB (EKG)
V1 QRS >0.12 or 120ms LBBB = negative QRS deflection RBBB = positive QRS deflection WALDO
55
Sgarbossa Criteria
Is LBBB causing MI? 1. Concordant ST elevation >1mm 2. ST depression >1mm in V1, V2, or V3 3. Discordant ST elevation >5mm ...negative deflected QS wave, and positive deflected ST segment Score greater than 3 is diagnostic for MI WALDO
56
De Winter's T wave (EKG)
Tall prominent T waves ...hyperacute T waves = ischemia Uploading ST segment depression >1mm Absence of ST segment elevation in precordial leads ST segment elevation in aVR Normal ST morphology WALDO
57
Out of hospital ROSC (EKG)
What prompted ROSC?? If pt received sodium bicarb then ROSC, they likely have a pH issue. WALDO
58
SHIP
Subtle inferior wall MIs Hyperacute T waves Isolated Posterior MIs
59
Subtle inferior wall MIs (EKG)
0.5mm ST depression in aVL is 97% accurate in identifying inferior wall MI Reciprocal changes in aVL should lead you to look down at lead III SHIP
60
Subtle high lateral wall MIs
Can be identified based on reciprocal changes - lead III Reciprocal changes in lead III should lead you to look at aVL SHIP
60
Hyperacute T waves (EKG)
First indicator of occlusionn short duration indication of ischemia SHIP
61
Isolated posterior MIs (EKG)
Isolated Posterior wall MI <3.3% of MIs Often paired w/inferior or lateral MI Reciprocal changes seen in V1-V4 Mirror image of anterior wall OMI SHIP
62
Agonists and antagonists
Agonists - occupy receptors and activate them Antagonists - occupy receptors but do not activate them. Antagonists block receptor activation by agonists.
63
Beta blockers
"-lol" drugs ie metoprolol, labetolol, propranolol Antagonists of the beta receptors in the heart and lungs. Slow HR, decrease BP
64
Esmolol
beta blocker antagonizes Beta-1 adrenergic receptors indications: SVT, uncontrolled HTN Adults: bolus w/500mcg/kg/min over 1 min then start infusion @50mcg/kg/min. Titrate q5min. Precautions: asthma, bradycardia, AV blocks, CHF.
65
labetalol
antihypertensive, non-selective beta antagonist. Adult dosing: 10-20mg slow IVP q10min up to max dose 300mg. Precautions: asthma, cariogenic shock, 1st degree heart block, severe bradycardia
66
Calcium channel blockers
Diltiazem, nicardipine (Cardene), nifedipine (Procardia) Blocks Ca++ influx into smooth muscle - vascular smooth muscle relaxation especially at coronary arteries. Slows impulses through SA and AV node
67
Nicardipine (Cardene)
Calcium channel blocker Indications: HTN Doses: adults start at 5mg/hr IV, increase by 2.5mg/hr q5-15 min to max 15 mg/hr Precautions: pregnancy, CHF
68
Clevidipine
Calcium channel blocker Antihypertensive, ischemic stroke HTN management Initial infusion 1-2mg/hr IV, titration of 1-2mghr will produce additional 2-4 mmHg decrease in SBP Precautions: soy or egg sensitivity
69
Vasopressors and Inotropes
Dopamine Epinephrine Dobutamine Norepinephrine Phenylephrine Vasopressin Vasopressor causes vasoconstriction Inotrope increases force of cardiac contraction.
70
Inopressors
Sympathomimetic (adrenergic) agents ...ie dopamine, norepinephrine Stimulate Beta 1 receptors, increase contractility, increase HR Indications: Acute LV failure, low CO states - low perfusion states, Vasogenic shock
71
Dopamine
Inopressor Increases contractility Increases cardiac output Increases renal perfusion 5-10mcg/kg/min most therapeutic more is NOT better
72
Norepinephrine (levophed)
Stimulates alpha adrenergic receptors Constriction of all vessels and increase in peripheral vascular resistance. Increases SBP and DBP Indications: vasogenic shock with tachycardia, sepsis, neurogenic shock. Dosing: 0.01-2mcg/kg/min or 2-30 mcg/min IV infusion
73
Inodilators
id dobutamine, milrinone Sympathomimetic (adrenergic) agents. Increase contractility Indications: acute LV failure, pulmonary vasoconstriction, low perfusion states.
74
Dobutamine
Inodilator Mild vasodilation Use caution in borderline hypotensive patients. Drops systemic vascular resistance Always fill the tank... Dosing: 2-20mcg/kg/min
75
Milrinone
Inodilator Indications: ischemic and non ischemic cardiomyopathy, CHF Dosing: 20mg/100ml NS or 40mg/100mL NS
76
Vasopressors
Vasopressin, Neo-synephrine, methylene blue Increase BP by constricting vessels Indications: profound neurogenic shock, push dose pressors, vasogenic shock, refractory septic shock.
77
phenylephrine
vasopressor Stimulates alpha receptors Increases BP without tachycardia Indications: vasogenic shock esp w/tachycardia, sepsis, neurogenic shock. Dosing: drip rate typically 10-100mcg/min loading dose followed by maintenance dose 40-60 mcg/min
78
Vasopressin
vasopressor Used in pts w/refractory shock despite adequate fluid resuscitation Indications: vasodilatory shock, septic shock Dosing: 0.01-0.04 units/min UGIB: 0.5 units/min
79
Methylene blue
vasopressor Indications: vasodilatory shock, septic shock Dosing 1.5-2 mg/kg over 20 min-1hr
80
Vasodilators
Action: venous - reduce preload arterial - reduce afterload. Indications: HTN, heart failure, cariogenic shock, CAD, PVD
81
hydralazine
vasodilator Directly dilates arterial system decreases afterload Indications: PIH, HTN Dosing: 5-10 mg IV
82
Nitroglycerin
vasodilator Dilates venous system (decreases preload) Higher doses dilate arterial system (decreases afterload), improves myocardial O2 consumption Indications: angina, MI Adult dosing: 0.5mg SL q5min OR 5mcg/min IV increasing by 5-20 mcg/minn q3-5 min
83
Nitroprusside
vasodilator Relaxes vascular smooth muscle Reduces preload and afterload Indications: HTN w/complications (hemorrhagic stroke), cariogenic shock, acute aortic dissection Precautions: pregnancy, cyanide toxicity Dosing: 0.5-10 mcg/kg/min titrated q5min
84
Heparinn
Indications: any condition caused by a blood clot (DVT, OMI, ischemic CVA, PE Precautions: recent major surgery, ulcer, GIB, renal dysfunction Dosing: Bolus 60-80 units/kg often max of 5k units, then infusion of 15-18 units/kg/hr
85
ALteplase (activase, t-PA)
Ischemic stroke STEMI PE dosing varies for each use
86
Axis deviation
Left axis - points away right axis - points together
87
Left axis pathologic
-31 to -90 degrees Rule out: LVH Left anterior fascicular block LBBB Inferior wall MI Paced rhythm
88
right axis deviation
+90 to +180 Chronic (old) RVH, COPD Lateral wall MI (pathologic Q waves) Left posterior hemi block Acute (new onset) Misplaced leads PE Sodium channel blocker OD ...TCAs, cocaine
89
Bi-fascicular block (meds)
Left anterior / left posterior block plus RBBB = bi-fascicular block RBBB is red flag for bi-fascicular block NEVER administer sodium channel blockers ...No Amiodarone, lidocaine, or procainamide Cardiovert (only) if necessary...no meds
90

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